Ulcer and gastritis

Recent progress in the area of ulcer and gastritis is still dominated by findings and reports on Helicobacter pylori and nonsteroidal anti-inflammatory drugs, which in turn are the two major causes of peptic ulcers. Although the prevalence of H. pylori is declining in most developed countries, it is still contributing to a significant proportion of peptic ulcers globally. The interrelationship of H. pylori gastritis in patients with gastroesophageal reflux has become more apparent. H. pylori-induced gastric body gastritis is associated with reduced acid production, and thus with reduced reflux and esophagitis. The controversies regarding the interactions between H. pylori and NSAIDs have still not been settled. With the availability of the new COX-2-specific inhibitors, the current scenario of NSAID-related gastroduodenal complications will certainly change. Short-term usage of these agents has significantly reduced the incidence of endoscopic ulcers, but the benefits in terms of clinical outcomes, such as bleeding or perforation, remain to be determined. This review summarizes the recent literature on peptic ulcer and gastritis.     

Current state and measures of NSAIDs induced ulcer

In recent years, the incidence of Helicobacter pylori (H. pylori) infection has been decreasing and the incidence of peptic ulcer and bleeding ulcer induced by NSAIDs, especially low-dose aspirin (LDA), have been increasing. PPI and PG are useful for treatment and prevention of ulcers in patients receiving continuous administration of NSAIDs and/or LDA. H. pylori eradication is effective if performed before the start of NSAIDs administration, but a beneficial effect of H. pylori eradication performed during NSAIDs treatment cannot be expected. The incidence of ulcers is lower when administering COX-2-selective inhibitor than when administering non-selective NSAIDs, but attention must be given to cardiovascular events as side effects when administering COX-2-selective inhibitor.     

Clinical features and diagnosis of non-steroidal anti-inflammatory drugs induced ulcers of the stomach

Helicobacter pylori (H. pylori) infection and non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin induce serious gastrointestinal ulcer and bleeding. Also both H. pylori infection and NSAIDs or aspirin use independently and significantly increase the risk of peptic ulcer and its complications. Interestingly, it has been reported that no evidence exists that reducing the dose or using modified release formulations such as enteric-coated of aspirin would reduce the incidence of ulcer bleeding. Selective COX-2 inhibitors use shows a low relative risk of ulcer bleeding than NSAIDs. However, when combined with aspirin, the differences between selective COX-2 inhibitors and NSAIDs tend to disappear. NSAIDs/aspirin dominantly develops multiple ulcers from the angulus to the antrum regardless of H. pylori infection. In contrast, the irregular shape of ulcer is more frequently detected in patients taking NSAIDs in comparison with H. pylori-associated ulcer, but the association was not seen in cases taking aspirin. This result indicates that the mechanism of ulcer formation may be different between NSAIDs and aspirin.     

雷贝拉唑与奥美拉唑三联疗法治疗幽门螺杆菌阳性消化性溃疡疗效比较--附40例分析

目的 :比较雷贝拉唑三联疗法与奥美拉唑三联疗法治疗幽门螺杆菌阳性消化性溃疡的疗效。方法 :将幽门螺杆菌阳性的消化性溃疡 85例分为两组 :治疗组 (雷贝拉唑三联疗法组 ) 4 0例 ,以雷贝拉唑 10mg、阿莫西林 10 0 0mg及甲硝唑 4 0 0mg每日 2次口服 ,治疗 1周后单独服用雷贝拉唑 10mg ,连服 7日 ;对照组 (奥美拉唑三联疗法组 ) 4 5例 :以奥美拉唑 10mg、阿莫西林 10 0 0mg及甲硝唑 4 0 0mg ,每日 2次口服 ,治疗 1周后单独服用奥美拉唑 10mg ,连服 7日。治疗期间每周门诊随诊 ,记录临床症状改善情况 ,用药结束 1个月后复查胃镜并检测幽门螺杆菌结果。结果 :治疗组和对照组治疗 1日的临床症状缓解率分别为 83%、 6 2 % ,差异有统计学意义 (P <0 0 5 ) ;1周后的症状缓解率均为 98%。治疗组和对照组的溃疡愈合率分别为 93%和 76 % ,差异有统计学意义 (P <0 0 5 ) ;治疗组和对照组的总有效率分别为 98%和 96 % ,差异无统计学意义 (P >0 0 5 )。治疗组和对照组的幽门螺杆菌根除率分别为 88%和 78% ,差异无统计学意义 (P >0 0 5 )。结论 :两组方案均能有效治疗消化性溃疡和缓解临床症状 ,并能有效地根除幽门螺杆菌。但雷贝拉唑三联疗法在快速改善临床症状和促进溃疡愈合方面优于奥美拉唑三联疗法。     

Pathologic condition and prognosis of NSAids ulcer

Recently, H. pylori infection rate has decreased and non-steroidal anti-inflammatory drugs(NSAIDs including aspirin) induced ulcers have increased more and more with aging in Japan. Pathological and clinical conditions of NSAIDs ulcer are different from that of H. pylori-related peptic ulcer. In other words, main pathologic condition of NSAIDs ulcer is not only gastric acid secretion but also destruction of defense mechanisms of upper gastrointestinal mucosa, because NSAIDs inhibit both cyclooxygenase (COX)-1 and COX-2 which block production of prostaglandins, consequently resulting in impairing gastroduodenal protective factors. Moreover, it is not rare that NSAIDs ulcer has serious complications such as bleeding and/or perforation. These should be paid attention in NSAIDs users in routine practice.     

Position of NSAIDs in causal factors of peptic ulcer

The cause of peptic ulcer is classified into five categories; infectious, drug-induced, hyperacidic, secondary, and idiopathic. Among these factors, H. pylori infection and non-steroidal anti-inflammatory drugs including aspirin (NSAIDs) are most important for development of gastroduodenal ulcer. More than 95 percent of gastroduodenal ulcers are associated with H. pylori or NSAIDs. Therefore, the frequency of non-H. pylori non-NSAIDs ulcer is very low. NSAIDs have the effect to inhibit synthesis of cyclooxygenase-1 (COX 1) and COX-2. This inhibitory action induces analgesic and anti-inflammatory effects. On the other hand, inhibitory action for COX-1 reduces the production of prostaglandin that is related to protective effect for gastrointestinal mucosa. Its mechanism is able to induce gastroduodenal ulcer. Since the elderly population in Japan is rising, the number of patients who need NSAIDs treatment is expected to increase in near future.     

雷贝拉唑与兰索拉唑三联疗法治疗幽门螺杆菌阳性消化性溃疡疗效比较

目的:比较雷贝拉唑三联疗法与兰索拉唑三联疗法治疗幽门螺杆菌阳性消化性溃疡的疗效。方法:将幽门螺杆菌阳性的消化性溃疡83例分为两组:治疗组(雷贝拉唑三联疗法组)41例,以雷贝拉唑10mg,阿莫西林1000mg及甲硝唑400mg每日2次口服,治疗1周后单独服用雷贝拉唑10mg,连服7d;对照组(兰索拉唑三联疗法组)42例:以兰索拉唑30mg,阿莫西林1000mg及甲硝唑400mg,每日2次口服,治疗1周后单独服用兰索拉唑30mg,连服7d。治疗期间每周门诊随诊,记录临床症状改善情况,用药结束1个月后复查胃镜并检测幽门螺杆菌结果。结果:治疗组和对照组1d的临床症状缓解率分别为80%、60%,差异有统计学意义(P<0.05);1周后症状缓解率均为98%。治疗组和对照组的溃疡愈合率分别为93%和76%,差异有统计学意义(P<0.05);治疗组和对照组的总有效率分别为98%和96%,差异无统计学意义(P>0.05)。治疗组和对照组的幽门螺杆菌根除率分别85%和81%,差异无统计学意义(P>0.05)。结论:两组方案均能有效治疗消化性溃疡和缓解临床症状,并能有效地根除幽门螺杆菌。但雷贝拉唑三联疗法在改善临床症状和促进溃疡愈合方面优于兰索拉唑三联疗法。     

Peptic ulcer pathophysiology

Despite extensive research, the etiology of peptic ulcer disease remains unclear. Given the multiple processes that control acid and pepsin secretion and defense and repair of the gastroduodenal mucosa, it is likely that the cause of ulceration differs between individuals. Acid and pepsin appear to be necessary but not sufficient ingredients in the ulcerative process. It is clear that the majority of gastric ulcers and a substantial number of duodenal ulcers do not have increased gastric acid secretion. Recent research has focused more on protection and repair of the stomach and duodenum. NSAIDs cause a significant number of gastric and duodenal ulcers; this is probably due to inhibition of prostaglandin production with loss of its protective effects. In the absence of NSAIDs and gastrinoma, it appears that most gastric ulcers and all duodenal ulcers occur in the setting of H. pylori infection. Evidence is mounting in support of H. pylori as a necessary ingredient in the ulcerative process, similar to acid and pepsin. It is not known whether the bacteria or the accompanying inflammation is the more important factor in the pathophysiology. Although the pathophysiology of gastric ulcer and duodenal ulcer is similar, there are clearly differences between the two groups. Duodenal ulcer is typified by H. pylori infection and duodenitis and in many cases impaired duodenal bicarbonate secretion in the face of moderate increases in acid and peptic activity. These facts suggest the following process: increased peptic activity coupled with decreased duodenal buffering capacity may lead to increased mucosal injury and result in gastric metaplasia. In the presence of antral H. pylori, the gastric metaplasia can become colonized and inflamed. The inflammation or the infection itself then disrupts the process of mucosal defense or regeneration resulting in ulceration. A cycle of further injury and increased inflammation with loss of the framework for regeneration may then cause a chronic ulcer. Gastric ulcer often occurs with decreased acid-peptic activity, suggesting that mucosal defensive impairments are more important. The combination of inflammation, protective deficiencies, and moderate amounts of acid and pepsin may be enough to induce ulceration. Many questions remain in understanding the pathophysiology of peptic ulcer disease. The physiology and pathophysiology of mucosal regeneration and the mechanisms by which H. pylori and inflammation disrupt normal gastroduodenal function will be fruitful areas of future investigation.     

消化性溃疡的复发与幽门螺杆菌感染168例分析

目的:观察消化性溃疡的复发与幽门螺杆菌(HP)感染的关系。方法:回顾性分析我院168例消化性溃疡病人的临床资料,从胃镜检查、碳14(一种检测HP的呼气试验)测试、病理组织活检及治疗后随访3年结果进行分析。结果:HP阳性率为82.8％,其中胃溃疡最高,为88.9％,其次为十二指肠球部溃疡、复合性溃疡、幽门前区溃疡,检出率分别为85.3％、60％、57.1％,经统计学处理P<0.01,提示HP感染与溃疡部位有相关性。随访发现溃疡病伴有HP感染的复发率较高,达30％,而单纯的消化性溃疡、无HP感染的3年复发率为5％左右。结论:HP感染是消化性溃疡复发的重要因素。     

Pathogenesis and therapy of gastric and duodenal ulcer disease

Despite the decreasing frequency of Helicobacter pylori-induced peptic ulcers, peptic ulcer disease remains a major clinical problem partly because nonsteroidal anti-inflammatory drug ulcers have increased in frequency. The reduction in nonsteroidal anti-inflammatory drug ulcers by use of selective cyclooxygenase-2 inhibitors will not eliminate the problem because of increased use of aspirin for cardiovascular prophylaxis. This article reviews current concepts of peptic ulcer pathogenesis and therapy according to ulcer etiology; discusses potential interactions between etiologies; and considers the therapy for H pylori infection including the effects of antimicrobial resistance, and the role of bismuth quadruple therapy or furazolidone salvage therapy.     

Ulcer and gastritis

The literature on peptic ulcer and gastritis in 2000 again focused on the topics of Helicobacter pylori, nonsteroidal anti-inflammatory drugs (NSAIDs), and gastric cancer. New diagnostic tests for H. pylori infection have been evaluated, and rescue therapies for failed H. pylori eradication have been tested. The causal relationship between H. pylori infection and nonulcer dyspepsia, gastric cancer, gastroesophageal reflux disease, and NSAID-related ulcers remained heated topics of debate. In 2000, landmark clinical trials and meta-analyses were published addressing these issues. The role of endoscopy in managing nonulcer dyspepsia was better defined. The role of H. pylori eradication in NSAID/aspirin users was reexamined in high-risk patients. Clinical benefit was finally confirmed for specific inhibitors of cyclooxygenase-2 (COX-2). The millennium year turned out to be a very important one in the advancement of knowledge in this field.     

Future for basic and clinical studies on peptic ulcer disease

Since the discovery of H. pylori, various causes of peptic ulcer disease is reevaluated, and only four factors are now considered most important; H. pylori infection, gastric acid, NSAID administration, and mental and physical stress. Among them, gastric acid is an aggravating factor, and gastric acid alone can hardly develop peptic ulcers. The relationship between H. pylori infection and stress has been studied at Hanshin-Awaji great earthquake occurred in 1995. Immediately after the earthquake, the number of patients with peptic ulcer disease has been greatly increased, and those patients were considered to be typical cases of stress ulcers. Interestingly, however, it was found that 83.2% of the patients were infected with H. pylori. The data suggested that stress ulcer developed in those infected with H. pylori. In contrast, the relationship between H. pylori infection and NSAID in the development of ulcer disease is more complex. It is still unclear whether H. pylori infection is an additive effect for development of peptic ulcer disease by NSAID administration or not.     

Ulcers and gastritis

This article reviews recently published reports on ulcers and gastritis. Helicobacter pylori is known to be an important pathogen involved in gastroduodenal inflammation and peptic ulcers. Conventional endoscopy is of limited usefulness in the evaluation of gastritis, but magnifying endoscopy is evidently helpful in the diagnosis of chronic atrophic gastritis, intestinal metaplasia, and H. pylori infection. A significant reduction in the incidence of refractory ulcers and the prevalence of H. pylori infection in patients with peptic ulcer disease followed the introduction of H. pylori eradication treatment. Chronic H. pylori infection is associated with gastric cancer, and the effect of H. pylori eradication on the prevention of gastric cancer is an important issue that is still a matter of controversy. Endoscopic hemostasis and intravenous proton-pump inhibitor (PPI) infusion represent a widely accepted approach to the treatment of peptic ulcer bleeding. In clinical practice, it is important to prevent recurrent bleeding and to treat patients who do not respond to endoscopic therapy or PPI treatment. Laparoscopic repair for peptic ulcer perforations, with postoperative eradication treatment, has gradually met with acceptance in patients with H. pylori infection. H. pylori infection and its treatment continue to be interesting problems in this field.     

非甾体类抗炎药物与消化性溃疡出血

目的：探讨非甾体类抗炎药物（NSAIDs）诱发消化性溃疡（peptic ulcer,PU）出血的临床流行病学特点。方法：调查我院1996年1月～2006年1月间因PU并出血收住院治疗患者的临床资料,根据入院前1周内有无服用NSAIDs史将患者分为2组,对2组病人的临床资料进行分析比较。结果：本研究共纳入1012例患者,其中服药组386例,未服药组626例。2组病人在性别、出血方式、既往PU史、胃及十二指肠溃疡的具体部位、糜烂,以及是否需要内镜治疗等方面的差异无显著性。但是服药组患者的年龄较未服药组更高;胃溃疡和复合溃疡、多发溃疡在服药组更多见（P〈0.05）。结论：应加强对NSAIDs相关性PU并出血临床特点的认识,尽量减少NSAIDs的不良反应。     

非甾体抗炎药相关性胃十二指肠溃疡并出血的临床特点及幽门螺杆菌对溃疡特点的影响

目的 研究非甾体技炎药(NSAIDs)所致胃十二指肠溃疡并出血的临床特点及幽门螺杆菌对溃疡特点的影响。方法 调查我院1997年1月至2001年12月间因胃十二指肠球部溃疡并出血收住院治疗患者的临床资料，根据入院前1周内有无服用NSAIDs史将患者分为两组，对两组患者的临床资料进行分析比较。结果 服药组86例，未服药组360例。服药组患者的年龄更高，血红蛋白下降更明显(P＝0．004)，胃溃疡和复合溃疡、多发溃疡及大溃疡在服药组更多见(P＜0．001)。未服药组幽门螺杆菌(Hp)的感染率为72．5％，服药组为53．4％(P＝0．001)。进一步的研究发现，Hp感染状态对NSAIDs相关溃疡并出血的临床特点无明显影响，但胃黏膜糜烂更常见(P＜0．05)。结论 应加强对NSAIDs相关性胃十二指肠溃疡并出血植床特点的认识，尽量减少NSAIDs的不良反应。     

Hypotheses on the role of cytokines in peptic ulcer disease

Helicobacter pylori is the cause of chronic type B gastritis and occurs in almost all patients with duodenal ulcers. Infection with H. pylori is characterized by an increased production of several inflammatory cytokines. Increasing evidence suggests a central role of these cytokines in the pathogenesis of H. pylori -associated gastritis and peptic ulcer disease. Cytokines may be crucial in the recruitment and activation of inflammatory cells and in stimulation of gastrin release. In addition to their proinflammatory properties, cytokines may also inhibit the ulcer occurrence by stimulation of prostaglandins and somatostatin release and by direct impairment of acid secretion. The balance of these factors may determine the clinical outcome of H. pylori infection.     

消化性溃疡幽门螺杆菌(Hp)清除前后血Hp抗体、PG、GAS 变化的研究

幽门螺杆菌(Helicobacter pylori,Hp)阳性消化性溃疡患者在Hp清除前后血清抗Hp-IgG,抗Hp-IgM,胃蛋白酶原(Pep-sinogen,PG)和胃泌素(Gastrin,GAS)水平如何?奥美拉唑,硫糖铝,罗红霉素治疗Hp感染的消化性溃疡的效果如何?本课题对上述问题进行了研究。1材料与方法1.1一般资料病例选     

Ulcers and gastritis

This article reviews recently published literature regarding ulcers and gastritis. Although endoscopy is the most useful procedure for diagnosis in the upper gastrointestinal tract, complications do occur, and procedure-related costs are significant. The appropriate indication for endoscopy has recently been debated. Helicobacter pylori is known to be an important pathogen involved in gastric and duodenal inflammation. Peptic ulcer disease and severe gastric mucosal injury are caused by virulent strains, and many reports have focused on CagA. Follow-up studies on surveillance endoscopy in patients with peptic ulcer or gastritis report that patients with atrophic gastritis and intestinal metaplasia are at significantly higher risk for gastric cancer. H. pylori eradication sometimes causes gastroduodenal erosion and reflux esophagitis, and the mechanisms involved have been revealed. Proton-pump inhibitors are useful in the treatment of ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs), reflux esophagitis, and for preventing rebleeding after endoscopic hemostasis, but the effect of long-term acid suppression on the gastric mucosa is still a matter of debate. H. pylori infection and NSAID intake are both risk factors for peptic ulcer disease, and are important aspects in this field.     

Influence of H. pylori infection on upper gastrointestinal damage

H. pylori infection and low-dose aspirin (LDA) are not only independent causal factors of peptic ulcer and gastrointestinal bleeding, they also have synergistic and additive effects. H. pylori infection rate has drastically decreased over the past decade to 34.3% amongst people in their 40's, 28.0% amongst those in their 30's, and 15.7% amongst those in their 20's. Therefore, LDA are expected to become more important factor of peptic ulcer in the near future. The incidence of peptic ulcer induced by LDA was 15.8% (16/101) in authors' hospital. Deep ulcers(more than proper muscularis layer) were only 4 cases, shallow ulcers(submucosal layer) were 12 cases. All deep ulcers were gastric ulcers (3 H. pylori positive, 1 negative), on the other hand shallow ulcers were 8 gastric ulcers (3 H. pylori positive, 5 negative), and 4 duodenal ulcers (1 H. pylori positive, 3 negative). Majority of peptic ulcers induced by LDA were shallow, and independent on H. pylori infection.     

雷贝拉唑与奥美拉唑三联疗法治疗老年性Hp阳性消化性溃疡疗效分析

目的观察雷贝拉唑与奥美拉唑治疗老年性消化性溃疡的临床疗效及安全性.方法将92例老年性消化性溃疡患者随机分为雷贝拉唑组（治疗组）46例,奥美拉唑组（对照组）46例.观察两组患者溃疡愈合率、幽门螺杆菌（Hp）根除率、不良反应等.结果雷贝拉唑组上腹疼痛消失率第1天为84.8%,第7天为95.7%,奥美拉唑组用药第1天为47.8%,第7天为76.1%,差异有统计学意义.观察组和对照组的溃疡愈合率分别为80.4%与52.2%,差异有统计学意义;观察组和对照组的总有效率分别为97.8%与82.6%,差异有统计学意义.治疗组和对照组的幽门螺杆菌根除率分别为84.8%与63.0%,差异有统计学意义.所有患者均未发现明显不良反应.结论雷贝拉唑和奥美拉唑治疗老年性消化性溃疡均有效安全,但雷贝拉唑在在缓解症状、促进溃疡愈合及根除幽门螺杆菌等方面均优于奥美拉唑.